目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1...目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1的胆固醇脂质体(1g/L)分别孵育2 h 后,用不同浓度 KCl(9-24)nmol/L,乙酰胆碱(10^(12)～10^(-6))mol/L 作用于平滑肌细胞,激动剂作用后30s,加入丙烯醛固定,分别测量各组细胞的收缩百分比.结果兔 SO 平滑肌细胞平均长度为(143.7±12.3)μm,经胆固醇脂质体作用后平均长度无明显变化,对 KCl 和乙酰胆碱呈浓度依赖性收缩.KCl(18mmol/L)诱导最大收缩比为22.2%±0.7%,而2:1的胆固醇脂质体作用后收缩比为16.5%±0.6%(P<0.01);乙酰胆碱(10^(-7)mol/L)诱导最大收缩比为20.3%±1.4%,2:1的胆固醇脂质体作用后收缩比为16.5%±1.3%(P<0.05).摩尔比为0.5:1胆固醇脂质体作用后最大收缩比分别为21.3%±1.4%和19.2%±1.1%,同对照组相比无显著下降.结论兔 SO 平滑肌细胞经摩尔比2:1的胆固醇脂质体后起收缩性下降,推测这是高胆固醇血症可以导致兔 SO 的动力异常的机制.展开更多
One-time injection of domestic preparation of bull parathyrin—parathyreoidin (1 U/100g body weight, intramuscular) leads to a significant decrease of the blood glucose level and an increase of the serum calcium level...One-time injection of domestic preparation of bull parathyrin—parathyreoidin (1 U/100g body weight, intramuscular) leads to a significant decrease of the blood glucose level and an increase of the serum calcium level in rats. There is a close negative correlation established between glucose and calcium level (r = ?0.813, P > 0.02). The calcium laktat load (9 mg) per os induces the same changes. There is a functional negative correlation established between glucose levels and total calcium content (r = ?0.997, P 0.01). It proves that the decrease of the blood glucose level under parathyrin injection is connected with hypercalcaemia. Parathyrin causes the reduction of the dynamics of hyperglycemia under the glucose load per os (30% solution, 1 ml/100g), i.e. parathyrin increases glucose tolerance. Glucose consumption by muscle (diaphragm) and adipose (epididymal) tissues in vivo and in vitro does not alter under parathyrin and it does not affect the stimulating effect of insulin on the process. The combinative effect of parathyrin and calcium channel blockers—isoptin (5 mg/kg, intraperitoneal) or nifedipin (1 mg/kg, intraperitoneal) reveals more intensive and lasting decrease of the blood glucose level in comparison with only parathyrin effect and more reduction of the dynamics of hyperglycemia under the glucose load. Thus, parathyrin decreases the blood glucose level, increases glucose tolerance and does not effect insulin resistance.展开更多
文摘目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1的胆固醇脂质体(1g/L)分别孵育2 h 后,用不同浓度 KCl(9-24)nmol/L,乙酰胆碱(10^(12)～10^(-6))mol/L 作用于平滑肌细胞,激动剂作用后30s,加入丙烯醛固定,分别测量各组细胞的收缩百分比.结果兔 SO 平滑肌细胞平均长度为(143.7±12.3)μm,经胆固醇脂质体作用后平均长度无明显变化,对 KCl 和乙酰胆碱呈浓度依赖性收缩.KCl(18mmol/L)诱导最大收缩比为22.2%±0.7%,而2:1的胆固醇脂质体作用后收缩比为16.5%±0.6%(P<0.01);乙酰胆碱(10^(-7)mol/L)诱导最大收缩比为20.3%±1.4%,2:1的胆固醇脂质体作用后收缩比为16.5%±1.3%(P<0.05).摩尔比为0.5:1胆固醇脂质体作用后最大收缩比分别为21.3%±1.4%和19.2%±1.1%,同对照组相比无显著下降.结论兔 SO 平滑肌细胞经摩尔比2:1的胆固醇脂质体后起收缩性下降,推测这是高胆固醇血症可以导致兔 SO 的动力异常的机制.
文摘One-time injection of domestic preparation of bull parathyrin—parathyreoidin (1 U/100g body weight, intramuscular) leads to a significant decrease of the blood glucose level and an increase of the serum calcium level in rats. There is a close negative correlation established between glucose and calcium level (r = ?0.813, P > 0.02). The calcium laktat load (9 mg) per os induces the same changes. There is a functional negative correlation established between glucose levels and total calcium content (r = ?0.997, P 0.01). It proves that the decrease of the blood glucose level under parathyrin injection is connected with hypercalcaemia. Parathyrin causes the reduction of the dynamics of hyperglycemia under the glucose load per os (30% solution, 1 ml/100g), i.e. parathyrin increases glucose tolerance. Glucose consumption by muscle (diaphragm) and adipose (epididymal) tissues in vivo and in vitro does not alter under parathyrin and it does not affect the stimulating effect of insulin on the process. The combinative effect of parathyrin and calcium channel blockers—isoptin (5 mg/kg, intraperitoneal) or nifedipin (1 mg/kg, intraperitoneal) reveals more intensive and lasting decrease of the blood glucose level in comparison with only parathyrin effect and more reduction of the dynamics of hyperglycemia under the glucose load. Thus, parathyrin decreases the blood glucose level, increases glucose tolerance and does not effect insulin resistance.
